Aldosterone induced by chronic stress promotes pancreatic steatosis in young male rats.

Aldosterone, a stress-related hormone, may contribute to pancreatic dysfunction. Its role in pancreatic physiology, inflammation, and fibrosis remains poorly understood. This study aimed to evaluate the effects of aldosterone on pancreatic histomorphology and islet cellularity under chronic stress conditions, and to determine whether eplerenone, a selective aldosterone receptor antagonist, can counteract them. Twenty-four young male Wistar rats were randomly divided into four groups (n = 6): control, chronic unpredictable mild stress (CUMS), control + vehicle (control + Veh), and CUMS + eplerenone (EP). Eplerenone was administered on postnatal day 51 via gastric tube 2 h before daily stress exposure for 4 weeks. Histological, immunohistochemical, and biochemical analyses were performed, including quantification of aldosterone, visceral adipose tissue, and pancreatic triacylglycerol. In CUMS group, the aldosterone level increased. In the exocrine pancreas, the aldosterone increased intralobular fat and triacylglycerol accumulation. Tumor necrosis factor alpha (TNFα)-positive necrotic acinar cells with pyknotic nuclei and perivascular fibrosis were evident. The endocrine pancreas exhibited increased inflammation and an altered distribution of islet sizes. Eplerenone reduced fat accumulation, inflammation, and exocrine structural damage but did not prevent TNF-α expression in islets. In conclusion, aldosterone induced by chronic stress contributes to pancreatic steatosis, and islet toxicity in young male rats, supporting aldosterone's pathogenic role.